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Jeffrey L Ardell - One of the best experts on this subject based on the ideXlab platform.

  • angiotensin receptors alter myocardial infarction induced remodeling of the guinea pig Cardiac Plexus
    American Journal of Physiology-regulatory Integrative and Comparative Physiology, 2015
    Co-Authors: Jean C Hardwick, Shannon E Ryan, Emily N Powers, Marie E Southerland, Jeffrey L Ardell
    Abstract:

    Neurohumoral remodeling is fundamental to the evolution of heart disease. This study examined the effects of chronic treatment with an ACE inhibitor (captopril, 3 mg·kg−1·day−1), AT1 receptor antagonist (losartan, 3 mg·kg−1·day−1), or AT2 receptor agonist (CGP42112A, 0.14 mg·kg−1·day−1) on remodeling of the guinea pig intrinsic Cardiac Plexus following chronic myocardial infarction (MI). MI was surgically induced and animals recovered for 6 or 7 wk, with or without drug treatment. Intracellular voltage recordings from whole mounts of the Cardiac Plexus were used to monitor changes in neuronal responses to norepinephrine (NE), muscarinic agonists (bethanechol), or ANG II. MI produced an increase in neuronal excitability with NE and a loss of sensitivity to ANG II. MI animals treated with captopril exhibited increased neuronal excitability with NE application, while MI animals treated with CGP42112A did not. Losartan treatment of MI animals did not alter excitability with NE compared with untreated MIs, but these animals did show an enhanced synaptic efficacy. This effect on synaptic function was likely due to presynaptic AT1 receptors, since ANG II was able to reduce output to nerve fiber stimulation in control animals, and this effect was prevented by inclusion of losartan in the bath solution. Analysis of AT receptor expression by Western blot showed a decrease in both AT1 and AT2 receptors with MI that was reversed by all three drug treatments. These data indicate that neuronal remodeling of the guinea pig Cardiac Plexus following MI is mediated, in part, by activation of both AT1 and AT2 receptors.

  • dynamic remodeling of the guinea pig intrinsic Cardiac Plexus induced by chronic myocardial infarction
    Autonomic Neuroscience: Basic and Clinical, 2014
    Co-Authors: Jean C Hardwick, Shannon E Ryan, Jeffrey L Ardell, Eric Beaumont, Marie E Southerland
    Abstract:

    Myocardial infarction (MI) is associated with remodeling of the heart and neurohumoral control systems. The objective of this study was to define time-dependent changes in intrinsic Cardiac (IC) neuronal excitability, synaptic efficacy, and neurochemical modulation following MI. MI was produced in guinea pigs by ligation of the coronary artery and associated vein on the dorsal surface of the heart. Animals were recovered for 4, 7, 14, or 50 days. Intracellular voltage recordings were obtained in whole mounts of the Cardiac neuronal Plexus to determine passive and active neuronal properties of IC neurons. Immunohistochemical analysis demonstrated an immediate and persistent increase in the percentage of IC neurons immunoreactive for neuronal nitric oxide synthase. Examination of individual neuronal properties demonstrated that afterhyperpolarizing potentials were significantly decreased in both amplitude and time course of recovery at 7 days post-MI. These parameters returned to control values by 50 days post-MI. Synaptic efficacy, as determined by the stimulation of axonal inputs, was enhanced at 7 days post-MI only. Neuronal excitability in absence of agonist challenge was unchanged following MI. Norepinephrine increased IC excitability to intracellular current injections, a response that was augmented post-MI. Angiotensin II potentiation of norepinephrine and bethanechol-induced excitability, evident in controls, was abolished post-MI. This study demonstrates that MI induces both persistent and transient changes in IC neuronal functions immediately following injury. Alterations in the IC neuronal network, which persist for weeks after the initial insult, may lead to alterations in autonomic signaling and Cardiac control.

  • remodeling of the guinea pig intrinsic Cardiac Plexus with chronic pressure overload
    American Journal of Physiology-regulatory Integrative and Comparative Physiology, 2009
    Co-Authors: Jean C Hardwick, Marie E Southerland, Caitlin N Baran, Jeffrey L Ardell
    Abstract:

    Chronic pressure overload (PO) is associated with Cardiac hypertrophy and altered autonomic control of Cardiac function, in which the latter may involve adaptations in central and/or peripheral Cardiac neural control mechanisms. To evaluate the specific remodeling of the intrinsic Cardiac nervous system following pressure overload, the descending thoracic aorta artery of the guinea pig was constricted ∼20%, and the animals recovered for 9 wk. Thereafter, atrial neurons of the intrinsic Cardiac Plexus were isolated for electrophysiological and immunohistochemical analyses. Intracellular voltage recordings from intrinsic Cardiac neurons demonstrated no significant changes in passive membrane properties or action potential depolarization compared with age-matched controls and sham-operated animals, but afterhyperpolarization duration was increased in PO animals. Neuronal excitability, as determined by the number of action potentials produced with depolarizing stimuli, was differentially increased in phasic neurons derived from PO animals in response to exogenously applied histamine compared with sham and age-matched controls. Conversely, pituitary adenylate cyclase-activating polypeptide-induced increases in intrinsic Cardiac neuron evoked AP frequency were similar between control and PO animals. Immunohistochemical analysis demonstrated a twofold increase in the percentage of neurons immunoreactive for neuronal nitric oxide synthase in PO animals compared with control. The density of mast cells within the intrinsic Cardiac Plexus from PO animals was also increased twofold compared with preparations from control animals. These results indicate that congestive heart failure associated with chronic pressure overload induces a differential remodeling of intrinsic Cardiac neurons and upregulation of neuronal responsiveness to specific neuromodulators.

  • chronic myocardial infarction induces phenotypic and functional remodeling in the guinea pig Cardiac Plexus
    American Journal of Physiology-regulatory Integrative and Comparative Physiology, 2008
    Co-Authors: Jean C Hardwick, Marie E Southerland, Jeffrey L Ardell
    Abstract:

    Chronic myocardial infarction (CMI) is associated with remodeling of the ventricle and evokes adaption in the Cardiac neurohumoral control systems. To evaluate the remodeling of the intrinsic Cardiac nervous system following myocardial infarction, the dorsal descending coronary artery was ligated in the guinea pig heart and the animals were allowed to recover for 7–9 wk. Thereafter, atrial neurons of the intrinsic Cardiac Plexus were isolated for electrophysiological and immunohistochemical analyses. Intracellular voltage recordings from intrinsic Cardiac neurons demonstrated no significant changes in passive membrane properties or action potential configuration compared with age-matched controls and sham-operated animals. The intrinsic Cardiac neurons from chronic infarcted hearts did demonstrate an increase in evoked action potential (AP) frequency (as determined by the number of APs produced with depolarizing stimuli) and an increase in responses to exogenously applied histamine compared with sham and age-matched controls. Conversely, pituitary adenylate cyclase-activating polypeptide (PACAP)-induced increases in intrinsic Cardiac neuron-evoked AP frequency were similar between control and CMI animals. Immunohistochemical analysis demonstrated a threefold increase in percentage of neurons immunoreactive for neuronal nitric oxide synthase (NOS) in CMI animals compared with control and the additional expression of inducible NOS by some neurons, which was not evident in control animals. Finally, the density of mast cells within the intrinsic Cardiac Plexus was increased threefold in preparations from CMI animals. These results indicate that CMI induces a differential remodeling of intrinsic Cardiac neurons and functional upregulation of neuronal responsiveness to specific neuromodulators.

Jean C Hardwick - One of the best experts on this subject based on the ideXlab platform.

  • angiotensin receptors alter myocardial infarction induced remodeling of the guinea pig Cardiac Plexus
    American Journal of Physiology-regulatory Integrative and Comparative Physiology, 2015
    Co-Authors: Jean C Hardwick, Shannon E Ryan, Emily N Powers, Marie E Southerland, Jeffrey L Ardell
    Abstract:

    Neurohumoral remodeling is fundamental to the evolution of heart disease. This study examined the effects of chronic treatment with an ACE inhibitor (captopril, 3 mg·kg−1·day−1), AT1 receptor antagonist (losartan, 3 mg·kg−1·day−1), or AT2 receptor agonist (CGP42112A, 0.14 mg·kg−1·day−1) on remodeling of the guinea pig intrinsic Cardiac Plexus following chronic myocardial infarction (MI). MI was surgically induced and animals recovered for 6 or 7 wk, with or without drug treatment. Intracellular voltage recordings from whole mounts of the Cardiac Plexus were used to monitor changes in neuronal responses to norepinephrine (NE), muscarinic agonists (bethanechol), or ANG II. MI produced an increase in neuronal excitability with NE and a loss of sensitivity to ANG II. MI animals treated with captopril exhibited increased neuronal excitability with NE application, while MI animals treated with CGP42112A did not. Losartan treatment of MI animals did not alter excitability with NE compared with untreated MIs, but these animals did show an enhanced synaptic efficacy. This effect on synaptic function was likely due to presynaptic AT1 receptors, since ANG II was able to reduce output to nerve fiber stimulation in control animals, and this effect was prevented by inclusion of losartan in the bath solution. Analysis of AT receptor expression by Western blot showed a decrease in both AT1 and AT2 receptors with MI that was reversed by all three drug treatments. These data indicate that neuronal remodeling of the guinea pig Cardiac Plexus following MI is mediated, in part, by activation of both AT1 and AT2 receptors.

  • dynamic remodeling of the guinea pig intrinsic Cardiac Plexus induced by chronic myocardial infarction
    Autonomic Neuroscience: Basic and Clinical, 2014
    Co-Authors: Jean C Hardwick, Shannon E Ryan, Jeffrey L Ardell, Eric Beaumont, Marie E Southerland
    Abstract:

    Myocardial infarction (MI) is associated with remodeling of the heart and neurohumoral control systems. The objective of this study was to define time-dependent changes in intrinsic Cardiac (IC) neuronal excitability, synaptic efficacy, and neurochemical modulation following MI. MI was produced in guinea pigs by ligation of the coronary artery and associated vein on the dorsal surface of the heart. Animals were recovered for 4, 7, 14, or 50 days. Intracellular voltage recordings were obtained in whole mounts of the Cardiac neuronal Plexus to determine passive and active neuronal properties of IC neurons. Immunohistochemical analysis demonstrated an immediate and persistent increase in the percentage of IC neurons immunoreactive for neuronal nitric oxide synthase. Examination of individual neuronal properties demonstrated that afterhyperpolarizing potentials were significantly decreased in both amplitude and time course of recovery at 7 days post-MI. These parameters returned to control values by 50 days post-MI. Synaptic efficacy, as determined by the stimulation of axonal inputs, was enhanced at 7 days post-MI only. Neuronal excitability in absence of agonist challenge was unchanged following MI. Norepinephrine increased IC excitability to intracellular current injections, a response that was augmented post-MI. Angiotensin II potentiation of norepinephrine and bethanechol-induced excitability, evident in controls, was abolished post-MI. This study demonstrates that MI induces both persistent and transient changes in IC neuronal functions immediately following injury. Alterations in the IC neuronal network, which persist for weeks after the initial insult, may lead to alterations in autonomic signaling and Cardiac control.

  • remodeling of the guinea pig intrinsic Cardiac Plexus with chronic pressure overload
    American Journal of Physiology-regulatory Integrative and Comparative Physiology, 2009
    Co-Authors: Jean C Hardwick, Marie E Southerland, Caitlin N Baran, Jeffrey L Ardell
    Abstract:

    Chronic pressure overload (PO) is associated with Cardiac hypertrophy and altered autonomic control of Cardiac function, in which the latter may involve adaptations in central and/or peripheral Cardiac neural control mechanisms. To evaluate the specific remodeling of the intrinsic Cardiac nervous system following pressure overload, the descending thoracic aorta artery of the guinea pig was constricted ∼20%, and the animals recovered for 9 wk. Thereafter, atrial neurons of the intrinsic Cardiac Plexus were isolated for electrophysiological and immunohistochemical analyses. Intracellular voltage recordings from intrinsic Cardiac neurons demonstrated no significant changes in passive membrane properties or action potential depolarization compared with age-matched controls and sham-operated animals, but afterhyperpolarization duration was increased in PO animals. Neuronal excitability, as determined by the number of action potentials produced with depolarizing stimuli, was differentially increased in phasic neurons derived from PO animals in response to exogenously applied histamine compared with sham and age-matched controls. Conversely, pituitary adenylate cyclase-activating polypeptide-induced increases in intrinsic Cardiac neuron evoked AP frequency were similar between control and PO animals. Immunohistochemical analysis demonstrated a twofold increase in the percentage of neurons immunoreactive for neuronal nitric oxide synthase in PO animals compared with control. The density of mast cells within the intrinsic Cardiac Plexus from PO animals was also increased twofold compared with preparations from control animals. These results indicate that congestive heart failure associated with chronic pressure overload induces a differential remodeling of intrinsic Cardiac neurons and upregulation of neuronal responsiveness to specific neuromodulators.

  • chronic myocardial infarction induces phenotypic and functional remodeling in the guinea pig Cardiac Plexus
    American Journal of Physiology-regulatory Integrative and Comparative Physiology, 2008
    Co-Authors: Jean C Hardwick, Marie E Southerland, Jeffrey L Ardell
    Abstract:

    Chronic myocardial infarction (CMI) is associated with remodeling of the ventricle and evokes adaption in the Cardiac neurohumoral control systems. To evaluate the remodeling of the intrinsic Cardiac nervous system following myocardial infarction, the dorsal descending coronary artery was ligated in the guinea pig heart and the animals were allowed to recover for 7–9 wk. Thereafter, atrial neurons of the intrinsic Cardiac Plexus were isolated for electrophysiological and immunohistochemical analyses. Intracellular voltage recordings from intrinsic Cardiac neurons demonstrated no significant changes in passive membrane properties or action potential configuration compared with age-matched controls and sham-operated animals. The intrinsic Cardiac neurons from chronic infarcted hearts did demonstrate an increase in evoked action potential (AP) frequency (as determined by the number of APs produced with depolarizing stimuli) and an increase in responses to exogenously applied histamine compared with sham and age-matched controls. Conversely, pituitary adenylate cyclase-activating polypeptide (PACAP)-induced increases in intrinsic Cardiac neuron-evoked AP frequency were similar between control and CMI animals. Immunohistochemical analysis demonstrated a threefold increase in percentage of neurons immunoreactive for neuronal nitric oxide synthase (NOS) in CMI animals compared with control and the additional expression of inducible NOS by some neurons, which was not evident in control animals. Finally, the density of mast cells within the intrinsic Cardiac Plexus was increased threefold in preparations from CMI animals. These results indicate that CMI induces a differential remodeling of intrinsic Cardiac neurons and functional upregulation of neuronal responsiveness to specific neuromodulators.

Marie E Southerland - One of the best experts on this subject based on the ideXlab platform.

  • angiotensin receptors alter myocardial infarction induced remodeling of the guinea pig Cardiac Plexus
    American Journal of Physiology-regulatory Integrative and Comparative Physiology, 2015
    Co-Authors: Jean C Hardwick, Shannon E Ryan, Emily N Powers, Marie E Southerland, Jeffrey L Ardell
    Abstract:

    Neurohumoral remodeling is fundamental to the evolution of heart disease. This study examined the effects of chronic treatment with an ACE inhibitor (captopril, 3 mg·kg−1·day−1), AT1 receptor antagonist (losartan, 3 mg·kg−1·day−1), or AT2 receptor agonist (CGP42112A, 0.14 mg·kg−1·day−1) on remodeling of the guinea pig intrinsic Cardiac Plexus following chronic myocardial infarction (MI). MI was surgically induced and animals recovered for 6 or 7 wk, with or without drug treatment. Intracellular voltage recordings from whole mounts of the Cardiac Plexus were used to monitor changes in neuronal responses to norepinephrine (NE), muscarinic agonists (bethanechol), or ANG II. MI produced an increase in neuronal excitability with NE and a loss of sensitivity to ANG II. MI animals treated with captopril exhibited increased neuronal excitability with NE application, while MI animals treated with CGP42112A did not. Losartan treatment of MI animals did not alter excitability with NE compared with untreated MIs, but these animals did show an enhanced synaptic efficacy. This effect on synaptic function was likely due to presynaptic AT1 receptors, since ANG II was able to reduce output to nerve fiber stimulation in control animals, and this effect was prevented by inclusion of losartan in the bath solution. Analysis of AT receptor expression by Western blot showed a decrease in both AT1 and AT2 receptors with MI that was reversed by all three drug treatments. These data indicate that neuronal remodeling of the guinea pig Cardiac Plexus following MI is mediated, in part, by activation of both AT1 and AT2 receptors.

  • dynamic remodeling of the guinea pig intrinsic Cardiac Plexus induced by chronic myocardial infarction
    Autonomic Neuroscience: Basic and Clinical, 2014
    Co-Authors: Jean C Hardwick, Shannon E Ryan, Jeffrey L Ardell, Eric Beaumont, Marie E Southerland
    Abstract:

    Myocardial infarction (MI) is associated with remodeling of the heart and neurohumoral control systems. The objective of this study was to define time-dependent changes in intrinsic Cardiac (IC) neuronal excitability, synaptic efficacy, and neurochemical modulation following MI. MI was produced in guinea pigs by ligation of the coronary artery and associated vein on the dorsal surface of the heart. Animals were recovered for 4, 7, 14, or 50 days. Intracellular voltage recordings were obtained in whole mounts of the Cardiac neuronal Plexus to determine passive and active neuronal properties of IC neurons. Immunohistochemical analysis demonstrated an immediate and persistent increase in the percentage of IC neurons immunoreactive for neuronal nitric oxide synthase. Examination of individual neuronal properties demonstrated that afterhyperpolarizing potentials were significantly decreased in both amplitude and time course of recovery at 7 days post-MI. These parameters returned to control values by 50 days post-MI. Synaptic efficacy, as determined by the stimulation of axonal inputs, was enhanced at 7 days post-MI only. Neuronal excitability in absence of agonist challenge was unchanged following MI. Norepinephrine increased IC excitability to intracellular current injections, a response that was augmented post-MI. Angiotensin II potentiation of norepinephrine and bethanechol-induced excitability, evident in controls, was abolished post-MI. This study demonstrates that MI induces both persistent and transient changes in IC neuronal functions immediately following injury. Alterations in the IC neuronal network, which persist for weeks after the initial insult, may lead to alterations in autonomic signaling and Cardiac control.

  • remodeling of the guinea pig intrinsic Cardiac Plexus with chronic pressure overload
    American Journal of Physiology-regulatory Integrative and Comparative Physiology, 2009
    Co-Authors: Jean C Hardwick, Marie E Southerland, Caitlin N Baran, Jeffrey L Ardell
    Abstract:

    Chronic pressure overload (PO) is associated with Cardiac hypertrophy and altered autonomic control of Cardiac function, in which the latter may involve adaptations in central and/or peripheral Cardiac neural control mechanisms. To evaluate the specific remodeling of the intrinsic Cardiac nervous system following pressure overload, the descending thoracic aorta artery of the guinea pig was constricted ∼20%, and the animals recovered for 9 wk. Thereafter, atrial neurons of the intrinsic Cardiac Plexus were isolated for electrophysiological and immunohistochemical analyses. Intracellular voltage recordings from intrinsic Cardiac neurons demonstrated no significant changes in passive membrane properties or action potential depolarization compared with age-matched controls and sham-operated animals, but afterhyperpolarization duration was increased in PO animals. Neuronal excitability, as determined by the number of action potentials produced with depolarizing stimuli, was differentially increased in phasic neurons derived from PO animals in response to exogenously applied histamine compared with sham and age-matched controls. Conversely, pituitary adenylate cyclase-activating polypeptide-induced increases in intrinsic Cardiac neuron evoked AP frequency were similar between control and PO animals. Immunohistochemical analysis demonstrated a twofold increase in the percentage of neurons immunoreactive for neuronal nitric oxide synthase in PO animals compared with control. The density of mast cells within the intrinsic Cardiac Plexus from PO animals was also increased twofold compared with preparations from control animals. These results indicate that congestive heart failure associated with chronic pressure overload induces a differential remodeling of intrinsic Cardiac neurons and upregulation of neuronal responsiveness to specific neuromodulators.

  • chronic myocardial infarction induces phenotypic and functional remodeling in the guinea pig Cardiac Plexus
    American Journal of Physiology-regulatory Integrative and Comparative Physiology, 2008
    Co-Authors: Jean C Hardwick, Marie E Southerland, Jeffrey L Ardell
    Abstract:

    Chronic myocardial infarction (CMI) is associated with remodeling of the ventricle and evokes adaption in the Cardiac neurohumoral control systems. To evaluate the remodeling of the intrinsic Cardiac nervous system following myocardial infarction, the dorsal descending coronary artery was ligated in the guinea pig heart and the animals were allowed to recover for 7–9 wk. Thereafter, atrial neurons of the intrinsic Cardiac Plexus were isolated for electrophysiological and immunohistochemical analyses. Intracellular voltage recordings from intrinsic Cardiac neurons demonstrated no significant changes in passive membrane properties or action potential configuration compared with age-matched controls and sham-operated animals. The intrinsic Cardiac neurons from chronic infarcted hearts did demonstrate an increase in evoked action potential (AP) frequency (as determined by the number of APs produced with depolarizing stimuli) and an increase in responses to exogenously applied histamine compared with sham and age-matched controls. Conversely, pituitary adenylate cyclase-activating polypeptide (PACAP)-induced increases in intrinsic Cardiac neuron-evoked AP frequency were similar between control and CMI animals. Immunohistochemical analysis demonstrated a threefold increase in percentage of neurons immunoreactive for neuronal nitric oxide synthase (NOS) in CMI animals compared with control and the additional expression of inducible NOS by some neurons, which was not evident in control animals. Finally, the density of mast cells within the intrinsic Cardiac Plexus was increased threefold in preparations from CMI animals. These results indicate that CMI induces a differential remodeling of intrinsic Cardiac neurons and functional upregulation of neuronal responsiveness to specific neuromodulators.

Shannon E Ryan - One of the best experts on this subject based on the ideXlab platform.

  • angiotensin receptors alter myocardial infarction induced remodeling of the guinea pig Cardiac Plexus
    American Journal of Physiology-regulatory Integrative and Comparative Physiology, 2015
    Co-Authors: Jean C Hardwick, Shannon E Ryan, Emily N Powers, Marie E Southerland, Jeffrey L Ardell
    Abstract:

    Neurohumoral remodeling is fundamental to the evolution of heart disease. This study examined the effects of chronic treatment with an ACE inhibitor (captopril, 3 mg·kg−1·day−1), AT1 receptor antagonist (losartan, 3 mg·kg−1·day−1), or AT2 receptor agonist (CGP42112A, 0.14 mg·kg−1·day−1) on remodeling of the guinea pig intrinsic Cardiac Plexus following chronic myocardial infarction (MI). MI was surgically induced and animals recovered for 6 or 7 wk, with or without drug treatment. Intracellular voltage recordings from whole mounts of the Cardiac Plexus were used to monitor changes in neuronal responses to norepinephrine (NE), muscarinic agonists (bethanechol), or ANG II. MI produced an increase in neuronal excitability with NE and a loss of sensitivity to ANG II. MI animals treated with captopril exhibited increased neuronal excitability with NE application, while MI animals treated with CGP42112A did not. Losartan treatment of MI animals did not alter excitability with NE compared with untreated MIs, but these animals did show an enhanced synaptic efficacy. This effect on synaptic function was likely due to presynaptic AT1 receptors, since ANG II was able to reduce output to nerve fiber stimulation in control animals, and this effect was prevented by inclusion of losartan in the bath solution. Analysis of AT receptor expression by Western blot showed a decrease in both AT1 and AT2 receptors with MI that was reversed by all three drug treatments. These data indicate that neuronal remodeling of the guinea pig Cardiac Plexus following MI is mediated, in part, by activation of both AT1 and AT2 receptors.

  • dynamic remodeling of the guinea pig intrinsic Cardiac Plexus induced by chronic myocardial infarction
    Autonomic Neuroscience: Basic and Clinical, 2014
    Co-Authors: Jean C Hardwick, Shannon E Ryan, Jeffrey L Ardell, Eric Beaumont, Marie E Southerland
    Abstract:

    Myocardial infarction (MI) is associated with remodeling of the heart and neurohumoral control systems. The objective of this study was to define time-dependent changes in intrinsic Cardiac (IC) neuronal excitability, synaptic efficacy, and neurochemical modulation following MI. MI was produced in guinea pigs by ligation of the coronary artery and associated vein on the dorsal surface of the heart. Animals were recovered for 4, 7, 14, or 50 days. Intracellular voltage recordings were obtained in whole mounts of the Cardiac neuronal Plexus to determine passive and active neuronal properties of IC neurons. Immunohistochemical analysis demonstrated an immediate and persistent increase in the percentage of IC neurons immunoreactive for neuronal nitric oxide synthase. Examination of individual neuronal properties demonstrated that afterhyperpolarizing potentials were significantly decreased in both amplitude and time course of recovery at 7 days post-MI. These parameters returned to control values by 50 days post-MI. Synaptic efficacy, as determined by the stimulation of axonal inputs, was enhanced at 7 days post-MI only. Neuronal excitability in absence of agonist challenge was unchanged following MI. Norepinephrine increased IC excitability to intracellular current injections, a response that was augmented post-MI. Angiotensin II potentiation of norepinephrine and bethanechol-induced excitability, evident in controls, was abolished post-MI. This study demonstrates that MI induces both persistent and transient changes in IC neuronal functions immediately following injury. Alterations in the IC neuronal network, which persist for weeks after the initial insult, may lead to alterations in autonomic signaling and Cardiac control.

Debora De Mello Goncales Santana - One of the best experts on this subject based on the ideXlab platform.

  • human apociii transgenic mice with epicardial adipose tissue inflammation and preservation of the Cardiac Plexus
    Experimental Gerontology, 2021
    Co-Authors: Diogo Rodrigues Jimenes, Andreia Vieira Pereira, Jairo Augusto Berti, Carmem Patricia Barbosa, Nilton Rodrigues Teixeira, Debora De Mello Goncales Santana
    Abstract:

    Hypertriglyceridemia is a result of the increase in the serum levels of lipoproteins, which are responsible for the transport of triglycerides and can be caused by genetic and/or metabolic factors. Animal models which either express or lack genes related to changes in the lipoproteins profile are useful to understand lipid metabolism. Apolipoprotein CIII (apoCIII) is an important modulator of hepatic production and peripheral removal of triglycerides. Mice that overexpress the apoCIII gene become hypertriglyceridemic, showing high concentrations of free fatty acids in the blood. Since hypertriglyceridemia is related to atherosclerosis, and the latter refers to Cardiac alterations, this study aimed at evaluating the morphological, morphometric and quantitative profiles of the Cardiac Plexus, as well as the morphometric and histopathological aspects of the epicardial adipose tissue in human apoCIII transgenic mice. Therefore, 8-12-month-old male C57BL/6 mice that overexpressed human apoCIII (CIII) and their respective controls were used. Our results showed that overexpression of human apoCIII did not modify morphological or quantitative parameters of Cardiac Plexus neurons; however, age increased both, the area and the number of such cells. Furthermore, there was a direct correlation of this dyslipidemia to the thickening of periganglionar type 1 collagens. On the other hand, this overexpression caused epicardial adipose tissue inflammation and an increase in the area of the adipocytes, thus, favoring the recruitment of inflammatory cells in this tissue. In conclusion, this overexpression is harmful since it is related to an increase in Cardiac adiposity, as well as to a predisposition to an inflammatory environment in the epicardial fat and to the incidence of cardiovascular diseases.

  • resistance training with and without insulin administration an analysis of the Cardiac Plexus and epicardial adipose tissue
    Research Society and Development, 2020
    Co-Authors: Diogo Rodrigues Jimenes, Victor Augusto Roncaglia Pereira, Andreia Vieira Pereira, Maria Montserrat Diaz Pedrosa, Jairo Augusto Berti, Debora De Mello Goncales Santana, Carmem Patricia Barbosa
    Abstract:

    The Cardiac Plexus is a vast network of neurons grouped into ganglia distributed throughout the myocardium. The epicardial adipose tissue covers the heart performing important functions, such as, lipid storage. However, its exaggerated expression might represent a risk factor, which can be prevented by the practice of physical activities that improves the heart contractile propulsive capacity. Insulin has been used in association with physical exercise so as to increase muscle mass and improve physical performance. Both insulin and exercise have been evidenced due to their neurotrophic effects. The purpose of this study was to ascertain whether insulin associated with resistance training could structurally modify the Cardiac Plexus and epicardial adipose tissue. Four groups (n = 6) of male Swiss mice were used: non-trained saline, non-trained insulin; trained saline; trained insulin. The training was performed on a vertical ladder at 90% of the maximum load, 3 times/week for 8 consecutive weeks. After the experimental period, the hearts of the animals were removed, and 5-μm sections were stained with Hematoxylin/Eosin, Giemsa and Picrossirius in order to evaluate the structures of the Cardiac Plexus. There was no significant difference with regard to the area and the total number of neurons, nor to the area with collagen. However, whereas insulin administration hypertrophied the adipocytes and predisposed an inflammatory environment, physical exercise played an anti-inflammatory role. As a conclusion, it is worth mentioning that resistance training did not change the Cardiac Plexus, however the epicardial adipose tissue was reduced, an effect antagonized by insulin.